Biomedical subjects

K Venkateswarlu

Publications and source records attributed to K Venkateswarlu.

At least 19 recordsLinked to original sources

PubMed2004

Impact of nitrophenols on the photosynthetic electron transport chain and ATP content in Nostoc muscorum and Chlorella vulgaris.

Concentration-dependent inhibition of the photosynthetic electron transport chain (photosystem I (PS I), photosystem II (PS II) and whole chain reaction) and ATP content was observed in Nostoc muscorum and Chlorella vulgaris grown with o-nitrophenol, m-nitrophenol, or 2,4-dinitrophenol. Although the extents of inhibition of the photosynthetic electron transport chain in both organisms were similar, PS II was more sensitive than PS I and whole chain reaction to the nitrophenols. Depletion of the ATP pool was noted in nitrophenol-grown cultures, probably as a consequence of nearly complete inhibition of the photosynthetic electron transport chain.

2,4-Dinitrophenol↗

PubMed2003

Effect of three nitrophenols on carbon metabolism in Nostoc muscorum and Chlorella vulgaris.

Carbon metabolism in selected strains of Nostoc muscorum and Chlorella vulgaris grown in the presence of three nitrophenols [o-nitrophenol, m-nitrophenol and 2,4-dinitrophenol] was assessed by examining activities of the enzymes such as amylase, starch phosphorylase, fructose 1,6-biphosphatase, sucrose phosphate synthase, and invertase. Marked alterations were observed in activities of the enzymes involved in starch metabolism. The cellular content of starch in nitrophenol-grown cultures was significantly reduced, whereas the levels of nonreducing and reducing sugars significantly increased. There was a significant increase in the activities of amylase and phosphorylase, and these alterations are probably responsible for the decreased amount of starch in the cultures. Furthermore, significant changes were noticed in activities of the enzymes involved in synthesis of sucrose as well.

Amylases↗

PubMed2003

Sequences associated with human iris pigmentation.

To determine whether and how common polymorphisms are associated with natural distributions of iris colors, we surveyed 851 individuals of mainly European descent at 335 SNP loci in 13 pigmentation genes and 419 other SNPs distributed throughout the genome and known or thought to be informative for certain elements of population structure. We identified numerous SNPs, haplotypes, and diplotypes (diploid pairs of haplotypes) within the OCA2, MYO5A, TYRP1, AIM, DCT, and TYR genes and the CYP1A2-15q22-ter, CYP1B1-2p21, CYP2C8-10q23, CYP2C9-10q24, and MAOA-Xp11.4 regions as significantly associated with iris colors. Half of the associated SNPs were located on chromosome 15, which corresponds with results that others have previously obtained from linkage analysis. We identified 5 additional genes (ASIP, MC1R, POMC, and SILV) and one additional region (GSTT2-22q11.23) with haplotype and/or diplotypes, but not individual SNP alleles associated with iris colors. For most of the genes, multilocus gene-wise genotype sequences were more strongly associated with iris colors than were haplotypes or SNP alleles. Diplotypes for these genes explain 15% of iris color variation. Apart from representing the first comprehensive candidate gene study for variable iris pigmentation and constituting a first step toward developing a classification model for the inference of iris color from DNA, our results suggest that cryptic population structure might serve as a leverage tool for complex trait gene mapping if genomes are screened with the appropriate ancestry informative markers.

Chromosomes, Human, Pair 10↗

PubMed2003

A classifier for the SNP-based inference of ancestry.

Ancestral inference from DNA could serve as an important adjunct for both standard and future human identity testing procedures. However, current STR methods for the inference of ancestral affiliation have inherent statistical and technical limitations. In an effort to identify bi-allelic markers that can be used to infer ancestral affiliation from DNA, we screened 211 SNPs in the human pigmentation and xenobiotic metabolism genes. Allele frequencies of 56 SNPs (most from pigmentation genes) were dramatically different between groups of unrelated individuals of Asian, African, and European descent, and both observed and simulated log likelihood ratios revealed that the markers were of exceptional value for ancestral inference. Log likelihood ratios of the multilocus estimates of biological ancestry (EAE/EBA) ranged from 7 to 10, which are on par with the best of the STR batteries yet described. A linear classification method was developed for incorporating these SNPs into a classifier model that was 99, 98, and 100% accurate for identifying individuals of European, African, and Asian descent, respectively. The methods and markers we describe are therefore an important first step for the development of a practical multiplex test for the inference of ancestry in a forensics setting.

Algorithms↗

PubMed2002

Functional coupling of rat metabotropic glutamate 1a receptors to phospholipase D in CHO cells: involvement of extracellular Ca2+, protein kinase C, tyrosine kinase and Rho-A.

We report here that metabotropic glutamate 1a (mGlu1a) receptors, stably expressed in CHO cells, stimulate phospholipase D (PLD) activity. Several mGlu receptor agonists were found to exert this effect, with a rank order of potency of: L-quisqualate>L-glutamate>(1S,3R)-1-aminocyclopentane-1,3-dicarboxylic acid [(1S,3R)-ACPD]=(S)-3,5-dihydroxyphenylglycine [(S)-DHPG]. Both L-glutamate- and (1S,3R)-ACPD-stimulated PLD activity were attenuated by the selective mGlu receptor antagonist (S)-alpha-methyl-4-carboxyphenylglycine. mGlu1a receptor-stimulated PLD was inhibited either by the selective protein kinase C (PKC) inhibitor, GF109203X, or via PKC downregulation. MGlu1a receptor-PLD coupling required extracellular Ca2+ and was sensitive to La3+ and Zn2+, inhibitors of intracellular Ca2+ store-operated Ca2+ influx. mGlu1a receptor-PLD coupling was inhibited by the selective tyrosine kinase inhibitor, genistein. In addition, mGlu1a receptor-PLD coupling was also inhibited by cell transfection with the selective Rho (small GTP-binding protein) inhibitors: C3-exoenzyme and dominant negative mutant RhoA constructs. Brefeldin A, a selective ADP-ribosylation factor (ARF) inhibitor, and a dominant negative ARF6 mutant, failed to significantly influence mGlu1a receptor-stimulated PLD activity. We conclude that mGlu1a receptors activate PLD via a mechanism that is dependent on extracellular Ca2+, PKC, tyrosine kinase and RhoA but independent of ARF.

Animals↗

PubMed2002

The physiology, pathophysiology and therapeutic potential of gap junctions in smooth muscle.

Phenotypic variability in smooth muscle cells accounts, in large part, for the incredible functional diversity required of the involuntary hollow organs of the body (i.e., respiratory passages, blood vessels, gastrointestinal tract, urogenital tract, etc.). In all instances coordination of smooth muscle cell responses, that is, contraction and relaxation, is critical to normal organ function. While numerous biological mechanisms exist for coordinating smooth muscle cell responses, intercellular communication through gap junctions represents a common denominator present in all organ systems. In this report, we review the evidence documenting the presence and functional significance of myocyte gap junctions to physiologically distinct organ systems, and furthermore, provide some examples of their putative roles in organ pathology. Finally, we advance the thesis that despite their ubiquity and heterogeneous expression, gap junctions are nonetheless potentially attractive therapeutic targets for the treatment of certain smooth muscle disorders. Their therapeutic efficacy will necessarily hinge on the existence of connexin isoform-selective junctional effects. The overall rationale for targeting the intercellular pathway is therefore analogous to strategies that target other ubiquitously expressed ion channels, such as calcium or potassium channels. Such strategies have proved efficacious for the treatment of a wide range of human smooth muscle disorders including hypertension, urinary incontinence and sexual function.

Animals↗

PubMed2002

Potassium channels and human corporeal smooth muscle cell tone: diabetes and relaxation of human corpus cavernosum smooth muscle by adenosine triphosphate sensitive potassium channel openers.

PURPOSE: Sustained contraction of human corporeal smooth muscle depends on continuous transmembrane calcium flux through voltage gated calcium channels. K channels modulate corporeal smooth muscle membrane potential and, thus, ultimately affect transmembrane calcium flux. Therefore, we characterized relaxation responses elicited by the K channel modulators pinacidil and levcromakalim on isolated human corporeal tissue strips. We also evaluated the possibility that there may be alterations in adenosine triphosphate sensitive K channel pharmacology/function related to the presence of diabetes mellitus. MATERIALS AND METHODS: A total of 215 isolated human corporeal tissue strips obtained from 57 male patients with organic erectile dysfunction were investigated. Cumulative concentration-response curves were constructed at half log increments for steady state relaxation responses elicited by pinacidil and levcromakalim on equivalently phenylephrine pre-contracted (to approximately 75% of maximum) isolated corporeal tissue strips. Potassium currents were measured using the cell attached whole cell patch clamp technique on freshly isolated corporeal smooth muscle cells. RESULTS: A concentration dependent, glibenclamide sensitive relaxation response of phenylephrine pre-contracted corporeal tissue strips was observed for pinacidil and levcromakalim. Consistent with such observations, electrophysiological recordings on freshly isolated myocytes revealed that pinacidil (10 microM.) and levcromakalim (10 microM.) induced whole cell potassium currents that were blocked by glibenclamide (10 microM.). In addition, statistical analysis revealed that phenylephrine pre-contracted corporeal tissue strips from patients without diabetes were more sensitive to relaxation by both compounds than corporeal tissue strips excised from those with diabetes. Furthermore, relaxation responses elicited by pinacidil and levcromakalim were not affected by charybdotoxin or 4-aminopyridine but were completely reversed by KCl or tetraethylammonium chloride. CONCLUSIONS: These data indicate that the adenosine triphosphate sensitive K channel subtype is likely to have an important role in the relaxation of isolated corporeal tissue strips and, moreover, they are the molecular target for the K channel modulators/openers levcromakalim and pinacidil. Such observations are consistent with the supposition that alterations in the structure/function/activity of these potassium channels may underlie at least some aspects of observed diabetes related differences in tissue sensitivity to K channel modulators.

Adenosine Triphosphate↗

PubMed2001

Human sterol 14alpha-demethylase activity is enhanced by the membrane-bound state of cytochrome b(5).

Human sterol 14alpha-demethylase (P45051; CYP51) catalyzes the oxidative removal of the C32 methyl group of dihydrolanosterol, an essential step in the cholesterol biosynthetic pathway. The reaction is dependent upon NADPH cytochrome P450 reductase (CPR) that donates the electrons for the catalytic cycle. Here we used a recombinant yeast CPR to investigate the abilities of four different forms of cytochrome b(5) to support sterol demethylation activity of CYP51. The cytochrome b(5) derivatives were genetically engineered forms of the native rat cytochrome b(5) core-tail: the soluble globular b(5) core (core), the core linked at its N-terminus with the secretory signal sequence of alkaline phosphatase (signal-core), and the signal sequence linked to the native b(5) (signal-core-tail). The rat core-tail enzyme greatly stimulated sterol demethylation, whereas the signal-core-tail was only marginally active. In contrast, the core and signal-core constructs were completely inactive in stimulating the demethylation reaction. Additionally, cytochrome b(5) enhanced sterol demethylation by more than threefold by accepting electrons from soluble yeast CPR and in its ability to reduce P450. We show that the nature of transient linkage between the hemoproteins and the redox partners is most likely brought about electrostatically, although productive interaction between cytochrome b(5) and CYP51 is governed by the membrane-insertable hydrophobic region in the cytochrome b(5) which in turn determines the correct spatial orientation of the core. This is the first report showing the stimulation of CYP51 by cytochrome b(5).

Amino Acid Sequence↗

PubMed2001

Activities and kinetic mechanisms of native and soluble NADPH-cytochrome P450 reductase.

Native yeast NADPH-cytochrome P450 oxidoreductase (CPR; EC 1.6.2.4) and a soluble derivative lacking 33 amino acids of the NH(2)-terminus have been overexpressed as recombinant proteins in Escherichia coli. The presence of a hexahistidine sequence at the N-terminus allowed protein purification in a single step using nickel-chelating affinity chromatography. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis confirmed the predicted molecular weights of the proteins and indicated a purity of >95%. Protein functionality was demonstrated by cytochrome c reduction and reconstitution of CYP61-mediated sterol Delta(22)-desaturation. Steady-state kinetics of cytochrome c reductase activity revealed a random Bi-Bi mechanism with NADPH donating electrons directly to CPR to produce a reduced intermediary form of the enzyme. The kinetic mechanism studies showed no difference between the two yeast CPRs in mechanism or after reconstitution with CYP61-mediated 22-desaturation, confirming that the retention of the NH(2)-terminable membrane anchor is functionally dispensable.

Cytochrome P-450 Enzyme System↗

PubMed2001

Casein kinase I associates with members of the centaurin-alpha family of phosphatidylinositol 3,4,5-trisphosphate-binding proteins.

Mammalian casein kinases I (CKI) belong to a family of serine/threonine protein kinases involved in diverse cellular processes including cell cycle progression, membrane trafficking, circadian rhythms, and Wnt signaling. Here we show that CKIalpha co-purifies with centaurin-alpha(1) in brain and that they interact in vitro and form a complex in cells. In addition, we show that the association is direct and occurs through the kinase domain of CKI within a loop comprising residues 217-233. These residues are well conserved in all members of the CKI family, and we show that centaurin-alpha(1) associates in vitro with all mammalian CKI isoforms. To date, CKIalpha represents the first protein partner identified for centaurin-alpha(1). However, our data suggest that centaurin-alpha(1) is not a substrate for CKIalpha and has no effect on CKIalpha activity. Centaurin-alpha(1) has been identified as a phosphatidylinositol 3,4,5-trisphosphate-binding protein. Centaurin-alpha(1) contains a cysteine-rich domain that is shared by members of a newly identified family of ADP-ribosylation factor guanosine trisphosphatase-activating proteins. These proteins are involved in membrane trafficking and actin cytoskeleton rearrangement, thus supporting a role for CKIalpha in these biological events.

Actins↗

PubMed2001

Phosphatidylinositol 3-kinase-dependent translocation of phospholipase Cgamma2 in mouse megakaryocytes is independent of Bruton tyrosine kinase translocation.

Activation of the collagen receptor glycoprotein VI (GPVI) by a collagen-related peptide (CRP) induces stimulation of platelets and megakaryocytes through the phosphatidylinositol (PI) 3-kinase-dependent pathway leading to activation of Bruton tyrosine kinase (Btk) and phospholipase Cgamma2 (PLCgamma2). Here, we present evidence that both proteins undergo PI 3-kinase-dependent translocation to the plasma membrane on CRP stimulation that is markedly inhibited by wortmannin and LY294002. Translocation of PLCgamma2 but not Btk is also seen in megakaryocytes from X-linked immunodeficiency mice, which have a mutation that reduces the affinity of the pleckstrin homology (PH) domain of Btk for PI 3,4,5-trisphosphate (PI 3,4,5-P3). Activation of PC12 cells by epidermal growth factor (EGF) results in increased PI 3-kinase activity and high PI 3,4,5-P3 levels that trigger translocation of the green fluorescent protein (GFP)-labeled PH of Btk, but not the GFP-labeled PH and tandem Src homology 2 (SH2) domains of PLCgamma2. In contrast to the results with CRP, the G protein-coupled receptor agonist thrombin stimulates PI 3-kinase-independent translocation of Btk but not PLCgamma2. In conclusion, these results demonstrate that in mouse megakaryocytes, CRP leads to PI 3-kinase-dependent translocation of PLCgamma2 and Btk that are independent of one another, whereas thrombin only induces translocation of Btk through a pathway that is independent of PI 3-kinase activity.

Agammaglobulinaemia Tyrosine Kinase↗

PubMed2001

Bladder injection of "naked" hSlo/pcDNA3 ameliorates detrusor hyperactivity in obstructed rats in vivo.

The goal of these studies was to examine the potential utility of bladder instilled K+ channel gene therapy with hSlo cDNA (i.e., the maxi-K channel) to ameliorate bladder overactivity in a rat model of partial urinary outlet obstruction. Twenty-two female Sprague-Dawley rats were subjected to partial urethral (i.e., outlet) obstruction, with 17 sham-operated control rats run in parallel. After 6 wk of obstruction, suprapubic catheters were surgically placed in the dome of the bladder in all rats. Twelve obstructed rats received bladder instillation of 100 microg of hSlo/pcDNA in 1 ml PBS during catheterization, and another 10 obstructed rats received 1 ml PBS (7 rats) or 1 ml PBS containing pcDNA only (3 rats). Two days after surgery cystometry was performed on all animals to examine the characteristics of the micturition reflex in conscious and unrestrained rats. Obstruction was associated with a three- to fourfold increase in bladder weight and alterations in virtually every micturition parameter estimate. PBS-injected obstructed rats routinely displayed spontaneous bladder contractions between micturitions. In contrast, hSlo injection eliminated the obstruction-associated bladder hyperactivity, without detectably affecting any other cystometric parameter. Presumably, expression of hSlo in rat bladder functionally antagonizes the increased contractility normally observed in obstructed animals and thereby ameliorates bladder overactivity. These initial observations indicate a potential utility of gene therapy for urinary incontinence.

Administration, Intravesical↗

PubMed2000

Signalling via ADP-ribosylation factor 6 lies downstream of phosphatidylinositide 3-kinase.

ADP-ribosylation factor (ARF) 6 regulates plasma membrane trafficking and cortical actin formation by cycling between inactive GDP and active GTP-bound conformations. Here we show that agonist stimulation of phosphatidylinositide 3-kinase (PI 3-kinase) activates a pathway that leads to ARF6 activation. We also describe experiments that propose a central role in this pathway for the PI 3-kinase-dependent plasma membrane recruitment of the cytohesin-1 family of PtdIns(3,4,5)P(3)-binding ARF-exchange factors.

ADP-Ribosylation Factor 6↗

PubMed2000

Analysis of synaptic quantal depolarizations in smooth muscle using the wavelet transform.

The time-frequency characteristics of synaptic potentials contain valuable information about the process of neurotransmission between nerves and their target organs. For example, at the synapse between autonomic nerves and smooth muscle, two central issues of neurophysiology, i.e., 1) the probability of neurotransmitter release and 2) the quantal behavior of transmission can be deduced from analysis of the rising phases of evoked excitatory junction potentials (eEJP's) recorded from smooth muscle. eEJP rising phases are marked by prominent inflexions, which reflect these features of neuronal activity. Since these inflexions contain time-varying frequency information, we have applied recent techniques of time-frequency analysis based upon wavelet transforms to eEJP's recorded from the guinea-pig vas deferens in vitro. We find that these techniques allow accurate and convenient characterization of neuronal release sites, and that their probability of release falls between 0.001-0.004. We have also analyzed eEJP's recorded in the presence of the chemical 1-heptanol, which reveals quantal depolarizations. These results have helped clarify the nature of the quantal depolarizations that underly eEJP's. The present method offers significant advantages over those previously employed for these tasks, and holds promise as a novel approach to the analysis of synaptic potentials.

Animals↗

PubMed2000

Neuromuscular blocking effects of an alkaloidal extract from Inula royleana: contractile and electrical studies on amphibian skeletal muscle in vitro.

The neuromuscular blocking properties of an alkaloidal extract from the root of Inula royleana have been investigated in vitro using a combination of mechanical and electrophysiological approaches. Neurogenic twitches of the frog sartorius were profoundly inhibited by concentrations of the extract > or = 20 micrograms/ml, being reduced to 50% of control amplitude in approximately 90 s at a concentration of > or = 20 micrograms/ml. They were partially reversed by neostigmine (6 micrograms/ml), and by prolonged washout of the extract. Muscle surface action potentials, recorded with extracellular electrodes, also declined rapidly in amplitude in the presence of the extract. Direct muscle stimulation during inhibition by the extract elicited contractions and action potentials whose magnitudes were similar to control responses. Resting membrane potentials, and the intracellular input impedance of the skeletal muscle cells, were not significantly changed by the alkaloids. These results indicate that the extract has significant neuromuscular blocking activity of a partially or slowly reversible nature. The block appears to be exerted at the postjunctional end-plate nicotine receptors, thus offering promise for the identification of novel cholinergic receptor antagonist(s).

Action Potentials↗

PubMed2000

Endosulfan poisoning--a clinical profile.

OBJECTIVES: The objective of the study is to identify the clinical profile of endosulfan poisoning and also to recognise any biochemical parameters which indicate clinical or subclinical dysfunction of organs so that the offending agent can be easily identified in a given case of poisoning and appropriate treatment instituted promptly. METHODS: Forty four individuals who consumed food which was accidentally contaminated by endosulfan in a rural area were the subjects of the present study. Except the one who died, rest 43 were examined by the authors. A details history, regarding the item of food taken and quantity consumed was noted. Routine bio-chemical parameters like CBC, blood urea, serum creatinine, serum electrolytes, LFT, S Calcium, S Phosporus, were estimated, in fourteen of the patients who were admitted into this hospital. In seven of the patients who were available for follow up, laboratory parameters which were abnormal initially were repeated. RESULTS: Examination revealed that vital signs were stable. There was no jaundice, central nervous system examination showed varying grades of altered sensorium, normal sized pupils briskly reacting to light, normal oculocephalic reflex. There were no lateralising signs like hemiparesis. Plantars were bilateral extensor. There were no signs of meningeal irritation. Complete blood counts, blood sugar, urea, serum creatinine, serum electrolytes were all normal. Liver function tests in the form of SGPT, SGOT were abnormal. Serum bilirubin levels were normal. The values of SGOT and SGPT returned to normal at the end of six weeks. All patients were treated symptomatically. A postmortem examination carried out on the individual who died due to status epilepticus confirmed that the death was due to asphyxia. CONCLUSIONS: Endosulfan poisoning can be suspected by the primary CNS manifestations with or without clinical or laboratory evidence of other organ dysfunction like liver, kidney and muscle.

Adolescent↗

PubMed1999

Confocal imaging of the subcellular distribution of phosphatidylinositol 3,4,5-trisphosphate in insulin- and PDGF-stimulated 3T3-L1 adipocytes.

The activation of phosphatidylinositol 3-kinase (PI 3-kinase) and production of PtdIns(3,4,5)P(3) is crucial in the actions of numerous extracellular stimuli, including insulin-stimulated glucose uptake. Platelet-derived growth factor (PDGF) also stimulates PI 3-kinase, but only weakly promotes glucose uptake when compared with insulin. Insulin and PDGF have thus been proposed to have differential effects on the subcellular targeting of PI 3-kinase. However, owing to a lack of suitable methodologies, the subcellular localization of the PtdIns(3,4,5)P(3) generated has not been examined. The pleckstrin-homology (PH) domains of the nucleotide exchange factors, ADP-ribosylation factor nucleotide-binding-site opener (ARNO) and general receptor for 3-phosphoinositides (GRP1), which have a high affinity and specificity for PtdIns(3,4,5)P(3), were fused to green fluorescent protein and used to examine the subcellular localization of PtdIns(3,4,5)P(3) generation in living 3T3-L1 adipocytes. PtdIns(3,4,5)P(3) was produced almost exclusively in the plasma membrane in response to both agonists, although the response to insulin was greater in magnitude and occurred in considerably more cells. The results suggest that the greater ability of insulin to stimulate glucose uptake may be the result of its ability to generate significantly more plasma-membrane PtdIns(3, 4,5)P(3) than PDGF. ARNO and GRP1 are nucleotide exchange factors for the small GTP-binding protein ADP-ribosylation factor 6 (ARF6). The inability of a constitutively active GTPase-deficient mutant of ARF6 (ARF6-Q67L; Gln(67)-->Leu) to cause glucose transporter GLUT4 translocation suggests that activation of this pathway is not sufficient to cause GLUT4 translocation.

3T3 Cells↗

PubMed1999

Quantal evoked depolarizations underlying the excitatory junction potential of the guinea-pig isolated vas deferens.

1. The effects of a putative gap junction uncoupling agent, heptanol, on the intracellularly recorded junction potentials of the guinea-pig isolated vas deferens have been investigated. 2. After the stimulation-evoked excitatory junction potentials (EJPs) had been suppressed by heptanol (2.0 mM) to undetectable levels, a different pattern of evoked activity ensued. This consisted of transient depolarizations that were similar to EJPs in being stimulus locked and in occurring at a fixed latency, but differed from EJPs in that they occurred intermittently and had considerably briefer time courses. 3. Analysis of the amplitudes and temporal parameters of the rapid residual depolarizations revealed a close similarity with spontaneous EJPs (SEJPs). There was no statistically significant difference between the rise times, time constants of decay and durations of the rapid residual depolarizations and of SEJPs. 4. Selected evoked depolarizations were virtually identical to SEJPs occurring in the same cell. Evoked depolarizations of closely similar amplitude and time course also occurred, usually within a few stimuli of each other. 5. These depolarizations appear to represent the individual quantal depolarizations that normally underlie the EJP and are therefore termed 'quantal excitatory junction potentials' (QEJPs) to distinguish them from both EJPs and SEJPs. 6. We examined the possibility that heptanol revealed QEJPs by disrupting electrical coupling between cells in the smooth muscle syncytium. Heptanol (2.0 mM) had no effect on the amplitude distribution, time courses, or the frequency of occurrence of SEJPs. Intracellular input impedance (Rin) of smooth muscle cells was left unaltered by heptanol. 7. 'Cable' potentials of the vas deferens, recorded using the partition stimulation method, also remained unchanged in the presence of heptanol. Thus, heptanol appeared not to modify syncytial electrical properties of the smooth muscle in any significant way. 8. Our observations show directly that the quantal depolarizations underlying the EJP in syncytial smooth muscle are SEJP-like events. However, no unequivocal statement can be made about the mechanism by which heptanol unmasks QEJPs from EJPs.

Animals↗